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Evidence-Based Complementary and Alternative Medicine
Volume 2016 (2016), Article ID 1042489, 9 pages
Research Article

Ligustrazine Inhibits Cartilage Endplate Hypertrophy via Suppression of TGF-β1

1Department of Orthopaedics & Traumatology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, No. 725 South Wanping Road, Shanghai 200032, China
2Institute of Spine, Shanghai University of Traditional Chinese Medicine, No. 725 South Wanping Road, Shanghai 200032, China
3Department of Orthopaedics, Sixth People’s Hospital, Jiaotong University, No. 600 Yi Shan Road, Shanghai 200233, China

Received 18 April 2016; Accepted 27 June 2016

Academic Editor: Hyunsu Bae

Copyright © 2016 Shufen Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


CEP hypertrophy is one of the characteristics of intervertebral disc degeneration (IDD). LIG exerts a protective effect on IDD in animal model. The effect of LIG on CEP hypertrophy is further investigated in the present study. Cells were isolated from hypertrophic samples obtained from patients during vertebral fusion surgery. Cellular proliferation and the expression of type I collagen (Col I) and TGF-β1 were tested. In the bipedal rats, the edges of the CEP and the sizes of noncartilaginous outgrowth, as well as the expression of osteogenic markers, Col1a, ALP, Runx2, and TGF-β1, were detected. Within two passages, the condensed hypertrophic CEP cells exhibited osteogenic capacity by bony-like nodules and ALP positive staining, along with increased expression of Col I and TGF-β1. LIG inhibited proliferation of CEP cells and downregulated the expression of Col I and TGF-β1 in vitro. Furthermore, LIG attenuated CEP hypertrophy on the lumbar spine of bipedal rats by reducing Col1a, ALP, Runx2, and TGF-β1 mRNA expression and TGF-β1 distribution in vivo. We concluded LIG exerted a preventive effect on CEP hypertrophy via suppression of TGF-β1 levels. This information could be used to develop alternative therapeutic methods to treat spinal CEP hypertrophy.